Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse

Freshly isolated adult mdx and nondystrophic (C57B110SnJ) muscle fibers were used to examine the potential role of resting Ca2+ influx in the pathogenesis of Duchenne and related dystrophies. Microfluorimetric determinations of resting divalent cation influx were obtained from undissociated intact m...

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Main Authors: C.George Carlson, Anton Gueorguiev, Diana M Roshek, Rebecca Ashmore, Jacquelyne S Chu, Judy E Anderson
Format: Article
Language:English
Published: Elsevier 2003-11-01
Series:Neurobiology of Disease
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996103001281
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spelling doaj-b92b84fc2ad84b4ca133b7a7fd813ce52021-03-20T04:48:42ZengElsevierNeurobiology of Disease1095-953X2003-11-01142229239Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouseC.George Carlson0Anton Gueorguiev1Diana M Roshek2Rebecca Ashmore3Jacquelyne S Chu4Judy E Anderson5Department of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaDepartment of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaDepartment of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaDepartment of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaDepartment of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaDepartment of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO 63501, USA; Department of Human Anatomy and Cell Science, University of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E OW3, CanadaFreshly isolated adult mdx and nondystrophic (C57B110SnJ) muscle fibers were used to examine the potential role of resting Ca2+ influx in the pathogenesis of Duchenne and related dystrophies. Microfluorimetric determinations of resting divalent cation influx were obtained from undissociated intact muscle fibers in the triangularis sterni (TS), a thin expiratory muscle. Morphological evidence indicated severe dystrophic alterations in the mdx TS at 5 months, and a prononunced loss of fibers with connective tissue infiltration in older animals. To examine resting Ca2+ influx, fibers were loaded with FURA PE3 and the rate of quenching of intracellular signal following the extracellular addition of Mn2+ was determined from extrajunctional regions. There was no significant difference in quench rate between nondystrophic and mdx TS fibers. These results indicate that severe dystrophic pathology in the absence of dystrophin is not due to generalized increases in resting Ca2+ influx.http://www.sciencedirect.com/science/article/pii/S0969996103001281Duchenne muscular dystrophymdx mouseDystrophinopathiesCalciumCalcium channelsMuscle necrosis
collection DOAJ
language English
format Article
sources DOAJ
author C.George Carlson
Anton Gueorguiev
Diana M Roshek
Rebecca Ashmore
Jacquelyne S Chu
Judy E Anderson
spellingShingle C.George Carlson
Anton Gueorguiev
Diana M Roshek
Rebecca Ashmore
Jacquelyne S Chu
Judy E Anderson
Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
Neurobiology of Disease
Duchenne muscular dystrophy
mdx mouse
Dystrophinopathies
Calcium
Calcium channels
Muscle necrosis
author_facet C.George Carlson
Anton Gueorguiev
Diana M Roshek
Rebecca Ashmore
Jacquelyne S Chu
Judy E Anderson
author_sort C.George Carlson
title Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
title_short Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
title_full Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
title_fullStr Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
title_full_unstemmed Extrajunctional resting Ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
title_sort extrajunctional resting ca2+ influx is not increased in a severely dystrophic expiratory muscle (triangularis sterni) of the mdx mouse
publisher Elsevier
series Neurobiology of Disease
issn 1095-953X
publishDate 2003-11-01
description Freshly isolated adult mdx and nondystrophic (C57B110SnJ) muscle fibers were used to examine the potential role of resting Ca2+ influx in the pathogenesis of Duchenne and related dystrophies. Microfluorimetric determinations of resting divalent cation influx were obtained from undissociated intact muscle fibers in the triangularis sterni (TS), a thin expiratory muscle. Morphological evidence indicated severe dystrophic alterations in the mdx TS at 5 months, and a prononunced loss of fibers with connective tissue infiltration in older animals. To examine resting Ca2+ influx, fibers were loaded with FURA PE3 and the rate of quenching of intracellular signal following the extracellular addition of Mn2+ was determined from extrajunctional regions. There was no significant difference in quench rate between nondystrophic and mdx TS fibers. These results indicate that severe dystrophic pathology in the absence of dystrophin is not due to generalized increases in resting Ca2+ influx.
topic Duchenne muscular dystrophy
mdx mouse
Dystrophinopathies
Calcium
Calcium channels
Muscle necrosis
url http://www.sciencedirect.com/science/article/pii/S0969996103001281
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